Cofilin is required for polarization of tension in stress fiber networks during migration
Year: 2020
Type: article
Abstract: Cell migration is associated with the establishment of defined leading and trailing edges, which in turn requires polarization of contractile forces. While the actomyosin stress fiber (SF) network plays a critical role in enforcing this polarity, precisely how this asymmetry is established remains unclear. Here, we provide evidence for a model in which the actin-severing protein cofilin (specifically cofilin-1) participates in symmetry breakage by removing low-tension actomyosin filaments during transverse arc assembly. Cofilin knockdown (KD) produces a non-polarized SF architecture that cannot be rescued with chemokines or asymmetric matrix patterns. Whereas cofilin KD increases whole-cell prestress, it decreases prestress within single SFs, implying an accumulation of low-tension SFs. This notion is supported by time-lapse imaging, which reveals weakly contractile and incompletely fused transverse arcs. Confocal and super-resolution imaging further associate this failed fusion with the presence of crosslinker-rich, tropomyosin-devoid nodes at the junctions of multiple transverse arc fragments and dorsal SFs. These results support a model in which cofilin facilitates the formation of high-tension transverse arcs, thereby promoting mechanical asymmetry.
Source: Journal of Cell Science
DOI: 10.1242/jcs.243873
Authors: Stacey Lee, Sanjay Kumar
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: green
Awards: Mechanical Regulation of Cell Shape and Migration by Actin Stress Fiber Subpopulations, A Zeiss Elyra S1 Structured Illumination Microscope for the Biological Imaging Fa, Genetic strategies for the quantitative control of cell-matrix mechanobiology, Biophysical Control of Cell Form and Function by Single Actomyosin Stress Fibers
OpenAlex ID: W3026425189